Intrauterine growth retardation: Altered hepatic energy and redox states in the fetal rat

Edward S. Ogata*, Sarah L. Swanson, James W Collins Jr, Sandra L. Finley

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

51 Scopus citations

Abstract

We determined the extent to which ligating both maternal uterine arteries affects fetal hepatic energy and redox states in the fetal rat. Bilateral maternal uterine artery ligation on d 18 of the rat's 21.5-d gestation signifinhibits fetal growth; sham surgery limits growth to a lesser extent. Within 12 h of surgery and persisting to d 19, small-for-gestational age (SGA) fetuses had significantly diminished ATP/ADP and adenylate charge ratios, whereas sham fetuses had values intermediate between SGA and normal. Hepatic mitochondrial redox state demonstrated similar changes. Cytosolic redox state in SGA fetuses at 12 and 24 h after surgery was significantly elevated. SGA fetuses had significantly diminished plasma insulin and elevated glucagon concentrations. On d 19 and 20, hepatic ATP/ADP and cytosolic NAD+/NADH correlated directly for sham and normal but not SGA fetuses. Alterations in glucose, insulin, and glucagon availability and hypoxia were responsible for the changes in energy and redox states. They may also have disassociated hepatic cytosolic from mitochondrial redox states and altered the equilibrium between adenine and nicotinamide nucleotides. These altered cellular functions retarded fetal growth. Newborn SGA, sham, and normal rat pups had similar hepatic ATP/ADP, cytosolic, and mitochondrial redox states at 10 and 240 min after delivery suggesting that the hypoglycemia which developed in SGA pups was not attributable to alterations in these variables.

Original languageEnglish (US)
Pages (from-to)52-55
Number of pages4
JournalPediatric research
Volume27
Issue number1
DOIs
StatePublished - Jan 1 1990

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health

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